These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Transforming growth factor-beta1 up-regulates the expression of nerve growth factor through mitogen-activated protein kinase signaling pathways in dental pulp cells.
    Author: Yongchaitrakul T, Pavasant P.
    Journal: Eur J Oral Sci; 2007 Feb; 115(1):57-63. PubMed ID: 17305717.
    Abstract:
    Transforming growth factor-beta1 (TGF-beta1) and nerve growth factor (NGF) have been detected in pulp tissues after injury and are implicated in the differentiation of odontoblast-like cells and in pulp tissue repair. We examined TGF-beta1-mediated regulation of NGF and investigated its signaling pathways in human dental pulp cells. Analyses by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) revealed that TGF-beta1 (1 ng ml(-1)) induced NGF mRNA and protein expression through the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK). Blockade of the p38 MAPK and JNK pathways with the respective upstream inhibitors (SB203580 and SP600125) abolished the TGF-beta1-mediated induction of NGF. In addition, SB225002, a G-protein-coupled receptor antagonist, and staurosporine, a serine-threonine kinase inhibitor, partially inhibited TGF-beta1-mediated induction of NGF. Phospho-p38 MAPK was suppressed by SB225002, whereas phospho-JNK was inhibited by staurosporine. We conclude that TGF-beta1 up-regulates NGF in human dental pulp cells. This suggests that TGF-beta1 plays a role in NGF regulation during pulp tissue repair. The signal of TGF-beta1 involves the activation of MAPK, especially p38 and JNK. We suggest that crosstalk between TGF-beta1 and G-protein-coupled receptor signaling also participates in the inductive mechanism.
    [Abstract] [Full Text] [Related] [New Search]